Open AccessHow the kidney hyperfiltrates in diabetes: From molecules to hemodynamics
Author(s) -
Tsuneo Takenaka,
Tsutomu Inoue,
Yusuke Watanabe
Publication year - 2015
Publication title -
world journal of diabetes
Language(s) - English
Resource type - Journals
ISSN - 1948-9358
DOI - 10.4239/wjd.v6.i4.576
Subject(s) - medicine , diabetes mellitus , glomerular hyperfiltration , renin–angiotensin system , juxtaglomerular apparatus , endocrinology , tubuloglomerular feedback , type 2 diabetes , afferent arterioles , kidney , angiotensin ii , diabetic nephropathy , blood pressure
In this review, we focused on two molecules, connexin and sodium-glucose cotransporter, which can link to diabetic hyperfiltration. In diabetic kidney, the activation of renin-angiotensin system occurs simultaneously with glomerular hyperfiltration. The latter largely depends on pathophysiological afferent arteriolar dilation in the presence of high angiotensin II. As a mechanistic basis for the above, tubular hypothesis has been proposed for type 1 diabetic patients as well as experimental models. Although tubular hypothesis has not been well evaluated in type 2 diabetes, clinical observations support that tubular hypothesis is true also in type 2 diabetes. Recent results on tubular hypothesis along with connexin abnormality in type 2 diabetes were revisited. In addition, the importance of sodium-glucose cotransporter in diabetic hyperfiltration is discussed. The link between salt paradox and the activation of renin-angiotensin system will be also reviewed.